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Arterial hypertension is associated with increased reactive oxygen species (ROS) formation which contributes to endothelium dysfunction and thereby diminish the vasorelaxant effects. Ginsenoside Rd, a purified component of the saponins found in P. notoginseng, has long been used for the treatment of cardiovascular diseases. In the present study, we investigated the effects of ginsenoside Rd on vascular endothelial dysfunction during hypertension and the underlying mechanisms.
Aortic arteries were isolated from 2-kidney 2-clip (2k2c) renovascular stroke-prone and angiotensin II (AngII)-induced hypertensive rats and normotensive rats. Blood pressure was measured by tail-cuff method with a Softron BP system. Contractile responses of rings were analyzed by myograph system. Reactive oxygen species were measured using dihydroethidium fluorescence imaging. NO production was determined using the fluorescent NO indicator DAF-2. Expression of NADPH oxidases was detected by western blot and immunofluroscence.
Ginsenoside Rd treatment significantly lowered the systolic blood pressure and concentration-dependently improved endothelium-dependent vascular relaxations and reduced the production of ROS in arterial rings from 2k2c and Ang II-induced hypertensive rats. Among the subunits of NADPH oxidases, the protein expression and activity of NOX1 and NOX2 was decreased in the aortas of ginsenoside Rd treated-hypertensive rats whereas the other isoforms were not significantly changed. Ginsenoside Rd inhibited angiotensin II-induced reduction of nitric oxide (NO) production and phosphorylation of eNOS in isolated aortic artery endothelia cells.
Ginsenoside Rd protected impaired endothelial function in hypertension through decreasing the expression of NOX1/2 NADPH oxidases and reducing ROS production. Our findings suggest that ginsenoside Rd may serve as new protective drug for the prevention of endothelial function by attenuating oxidative stress during hypertension.